Coverage Policy Manual
Policy #: 1997201
Category: Medicine
Initiated: July 1993
Last Review: September 2018
  EKG, Signal Averaged

Description: Signal-averaged electrocardiography (SAECG) is a technique involving computerized analysis of small segments of a standard EKG to detect abnormalities, termed "ventricular late potentials" (VLP), that would be otherwise obscured by “background” skeletal muscle activity. VLPs reflect aberrant, asynchronous electrical impulses arising from viable isolated cardiac muscle bordering an infarcted area and are thought to be responsible for ventricular tachyarrhythmias. Therefore, VLPs, as measured by SAECG, have been investigated as a risk factor for arrhythmic events in patients with a variety of cardiac conditions, including cardiomyopathy and prior history of myocardial infarction (MI). Patients considered being at high risk of ventricular arrhythmias and thus sudden death may be treated with drugs to suppress the emergence of arrhythmias or automatic implantable cardiac defibrillators (AICD) to promptly detect and terminate tachyarrhythmias when they occur. Since sudden cardiac death, whether from arrhythmias or pump failure, is one of the most common causes of death after a previous myocardial infarction, there is intense interest in risk stratification to target therapy. Patient groups are divided into those who have not experienced a life-threatening arrhythmia (i.e., primary prevention) and those who have (i.e., secondary prevention). SAECG is just one of many risk factors that have been investigated. Others include left ventricular ejection fraction, arrhythmias detected on Holter monitor or electrophysiologic studies, heart rate variability, and baroreceptor sensitivity. T-wave alternans is another technique for risk stratification. T-wave alternans, addressed separately in policy 2002016, measures beat-to-beat variability, while SAECG measures beat-averaged conduction.

Signal averaged electrocardiography (SAECG) for use including, but not limited to, a technique of risk stratification for arrhythmias after prior myocardial infarction; in patients with cardiomyopathy; in patients with syncope; as an assessment of success after surgery for arrhythmia; in the detection of acute rejection of heart transplants; as an assessment of efficacy of antiarrhythmic drug therapy; or in the assessment of success of pharmacological, mechanical, or surgical interventions to restore coronary blood flow is not covered for members covered  based on benefit certificate primary coverage criteria that requires scientific evidence of effectiveness.

For members with contracts without primary coverage criteria, signal averaged electrocardiography (SAECG) is considered investigational and is not covered for use including, but not limited to, as a technique of risk stratification for arrhythmias after prior myocardial infarction; in patients with cardiomyopathy; in patients with syncope; as an assessment of success after surgery for arrhythmia; in the detection of acute rejection of heart transplants; as an assessment of efficacy of antiarrhythmic drug therapy; or in the assessment of success of pharmacological, mechanical, or surgical interventions to restore coronary blood flow.  Investigational services are exclusions in the member benefit contract.

Signal-averaged electrocardiography has been thoroughly studied as a risk stratification tool for potentially fatal arrhythmias in patients with a previous myocardial infarction (MI). As reviewed by the Agency for Health Care Policy and Research (AHCPR) in 1998, SAECG is associated with a low positive predictive value ranging from 8%–44%, depending on the population studied.  In contrast, the negative predictive value (i.e., the ability to identify those patients who will not experience ventricular arrhythmias) ranges from 88%–97%, suggesting that the negative predictive value may be used to identify patients who would not benefit from antiarrhythmic therapy. However, a key statistic underlying the negative predictive value is the underlying prevalence of the outcome. Although sudden cardiac death is the most common cause of death in the 1-year period after infarction, it is relatively uncommon (2.5%–11.3%) and declining, due to increasing use of thrombolytic therapy, aspirin, and beta-blockers.  Thus, given the relative low incidence of arrhythmias, the high negative predictive value is not surprising.
In 1996, the American College of Cardiology published an expert consensus document that concluded that SAECG had an established or valuable role in clinical care in the following situations:
    • Stratification of risk of developing sustained ventricular arrhythmias in patients recovering from MI who are in sinus rhythm without electrocardiographic evidence of bundle branch block or intraventricular conduction delay
    • Identification of patients with ischemic heart disease and unexplained syncope who are likely to have inducible sustained ventricular tachycardia
    • Stratification of risk of developing sustained ventricular arrhythmia in patients with nonischemic cardiomyopathy
    • Assessment of success of operation for sustained ventricular tachycardia
However, the ultimate validation of any diagnostic test is to determine how it is used in the management of patients, and whether the management decisions result in improved health outcomes. The following discussion focuses on the clinical use of SAECG as reported in clinical trials of antiarrhythmic therapies.
Over the past two decades, a large number of randomized clinical trials have evaluated the effectiveness of either antiarrhythmic drugs or AICD implantation in post-MI patients. These trials have generally used a variety of risk stratification criteria to positively select patients for intervention. By selecting patients with a sufficiently high risk of arrhythmia, the benefits of treating arrhythmia will hopefully outweigh any adverse effects of the treatment. For the purposes of this discussion, the most relevant studies are those that look at patients who have not experienced a prior episode of near fatal ventricular arrhythmia or aborted sudden death. Patients with a prior history of a potentially fatal arrhythmia are already at sufficiently high risk and are considered candidates for either antiarrhythmic therapy or AICD.
Initially it was thought that pharmacological suppression of premature ventricular contractions (PVCs), identified on post-MI monitoring, would reduce the incidence of subsequent sustained, symptomatic arrhythmias. The Cardiac Arrhythmia Suppression Trial (CAST) was a placebo-controlled, randomized trial that tested the efficacy of either encainide, flecainide, or moricizine in reducing arrhythmic death in patients with a lowered ejection fraction and 6 or more PVCs per hour.  CAST was terminated prematurely when an interim analysis suggested that the drug therapy was associated with an increase in the incidence in arrhythmic death. This trial raised concerns about proarrhythmic effects of antiarrhythmic drugs and has lead to caution in the use of any antiarrhythmic drug therapy.
The drugs in the CAST trial are known as class I antiarrhythmics, defined as those agents that slow conduction. After the failure of the CAST trial, research was focused on class III agents, which prolong repolarization. The most commonly researched member of this class of drugs is amiodarone. There have been a number of small randomized studies of amiodarone, but the largest are the EMIAT (European Myocardial Infarct Amiodarone Trial) and CAMIAT (Canadian Amiodarone Myocardial Infarction Arrhythmia Trial), both of which assessed the effect of amiodarone on mortality in patients with high-risk markers after MI.   In the EMIAT trial, patients with a history of MI were stratified according to their ejection fraction. In the CAMIAT trial, patients were recruited based on results of Holter monitoring. Therefore, neither of these key trials used SAECG as a patient selection criterion.
The results of both of these trials suggested that while amiodarone was associated with a decreased risk of arrhythmias, there was no overall reduction in all-cause mortality. Therefore, the major finding of these trials focused on the safety of amiodarone, in contrast to the class I agents studied in the CAST trial. The clinical effectiveness of amiodarone is less certain and may be associated with a reduction of morbidity and quality of life associated with symptomatic arrhythmias, although this outcome has not been specifically studied. It is possible that a normal SAECG could be considered to deselect patients who would be unlikely to benefit from amiodarone therapy. However, this outcome has not been specifically studied, particularly since the overall benefit of amiodarone therapy is still controversial.
With the somewhat disappointing results of these drug trials, attention has turned toward the use of AICDs, particularly as these devices have become more sophisticated. Early generations of AICDs required thoracotomy for insertion but miniaturization has permitted outpatient insertion with the use of local anesthesia. With this reduction in the risk associated with AICDs, there was an interest in exploring their use in patients without a prior history of sustained, symptomatic ventricular arrhythmias. Several randomized studies have now been completed. The MADIT trial recruited post-MI patients with left ventricular ejection fraction of less than 35%, non-sustained ventricular tachycardia identified on Holter monitoring or stress test, and inducible, procainide-resistant, sustained ventricular arrhythmia on electrophysiologic study (EPS).  These characteristics were thought to identify a very high risk group for ventricular arrhythmias, in part due to the desire to have very high event rates to increase the power of the trial. The MADIT trial reported a marked reduction in mortality in those receiving a defibrillator compared to patients treated conventionally, mostly with amiodarone. Following the publication of the results, the U.S. Food and Drug Administration (FDA) approved expanded labeling for defibrillators in patients who met the MADIT criteria, Medicare announced coverage for AICD in this patient population, and the American College of Cardiology (ACC) has published guidelines endorsing the study results. As noted above, SAECG was not used as a patient selection criterion, and thus is not included as a recommended test as part of the ACC guidelines.
In contrast to the other trials reviewed above, the CABG-Patch trial used SAECG as a positive patient selection criterion.  The CABG-Patch trial recruited patients scheduled for a CABG who had an ejection fraction of less than 36% and abnormalities on the SAECG. The use of an SAECG was based on a pilot study that showed an abnormal SAECG was associated with a mortality rate that was double that seen in those with a normal SAECG in the 2 years after CABG.  Patients were randomized to a defibrillator group or a control group, and all received CABG. After an average follow-up of 32 months, there was no evidence of improved survival among those in the defibrillator group. However, it cannot be determined whether the failure of this trial was due to the selection criteria or the treatments being compared.
Therefore, based on the above review, it can be seen that the SAECG has not been successfully used as a patient selection criterion in the critical randomized trials investigating both drug and device antiarrhythmic therapy in the post-MI patient. In the majority of trials, it has not been included as a patient selection criterion, and the one trial in which it was used reported negative results.
2006 Update
A search of the literature based on the MEDLINE database was performed for the period of 1999 through January 2006. More recent trials investigating the use of AICD in post-MI patients have not provided clarity regarding the issue of risk stratification. The MADIT-II trial selected patients solely on the basis of left ventricle ejection fraction and showed a survival benefit among those randomized to AICD.  Grimm and colleagues reported on the results of the Marburg Cardiomyopathy study, a prospective observational study designed to determine the clinical value of potential noninvasive arrhythmia risk predictors among 343 patients with idiopathic dilated cardiomyopathy and followed up for 52 +/- 21 months for major arrhythmic events.  Reduced LV ejection fraction and lack of beta blocker use were important risk factors, but results of SAECG and T-wave alternans were not. Results of SAECG were found to only be a weak predictor of sudden cardiac death in a consecutive series of 700 patients with a history of acute myocardial infarction (AMI).  In another study of 1,800 consecutive survivors of AMI who underwent reperfusion therapy, late potentials identified by SAECG were not significantly associated with the endpoints of cardiac death or serious arrhythmias. No additional data have directly linked risk stratification information provided by SAECG to improved patient outcomes, improved efficiency, or reduced costs.
There are inadequate data to evaluate the impact on patient management of other applications of SAECG including, but not limited to, its use in patients with cardiomyopathy; assessment of success after surgery for arrhythmia; detection of acute rejection of heart transplants; assessment of efficacy of antiarrhythmic drug therapy; assessment of success of pharmacological, mechanical, or surgical interventions to restore coronary artery blood flow; or risk stratification of patients with Brugada syndrome. Regarding the use of SAECG to identify patients with syncope who may have inducible ventricular tachycardia, even though the American College of Cardiology consensus document concluded that SAECG had an established role, data within that report reported only modest sensitivity (73%) and poor positive predictive values.  Thus the test, if used as a screening test to determine who should have electrophysiologic studies, will fail to detect many patients who have positive electrophysiologic studies.
2007 Update
A literature search was conducted using MEDLINE through June 2007. None of the articles identified would lead to a change in the policy statement. No trials were found where prospective use of SAECG was shown to improve outcomes. Thus, the policy statement remains unchanged.
2008 Update
From the 2008 Scientific Statement on risk stratification (Goldberger, 2008):
Abundant data show that an abnormal SAECG may identify patients with prior MI at risk for SCD. Given the high negative predictive value of this test, it may be useful for the identification of patients at low risk. Routine use of the SAECG to identify patients at high risk for SCD is not adequately supported at this time. Further studies are required to assess the utility of this test.
The policy was updated with a literature review through December 2010. No studies involving large numbers of patients were identified that used SAECG prospectively to improve outcomes. Thus, the major limitation of existing data, as noted in prior updates, remains and the policy statement is unchanged.
One study from Japan evaluated the use of SAECG in a study of 222 hospitalized patients found to have non-sustained ventricular tachycardia. Forty-three patients with ischemic heart disease and 50 with non-ischemic cardiomyopathy were evaluated using an algorithm for risk-stratification (Ueno, 2007). The algorithm included left ventricular ejection fraction, signal-averaged electrocardiography (in 69 patients), programmed ventricular stimulation, and family history of sudden cardiac death; in follow-up, programmed stimulation was done for all positive SAECG studies. Of the 222 patients, 151 (68.0%) were successfully risk-stratified and 32 patients consequently received an ICD (21.2% of the algorithm). The remaining 119 patients without an ICD (algorithm-observation group) were observed. During an average of 28 months of follow-up, the patients in the algorithm-ICD group had a significantly higher prevalence of tachyarrhythmic events than those in the algorithm-observation group (9/32 vs. 1/119; p<0.05). In the algorithm-ICD group, 2, 1, and 6 patients experienced sudden cardiac death, aborted sudden cardiac death, and appropriate ICD intervention, respectively. The authors concluded that this proposed algorithm for risk-stratification of patients with non-sustained ventricular tachycardia may be feasible for appropriate selection of candidates for prophylactic ICD implantation.
As part of this update, a prior analysis by Bailey and colleagues of the utility of tests for risk stratification was added to the policy (Bailey, 2001). This study reviewed 44 reports for which values of major arrhythmic events (MAE) and predictive accuracy of several tests (signal-averaged electrocardiography, heart rate variability, severe ventricular arrhythmia on ambulatory electrocardiography, left ventricular ejection fraction, and electrophysiological studies [EPS]) could be inferred. A meta-analysis of reports used receiver-operating characteristic curves to estimate mean values for sensitivity and specificity for each test, and 95% confidence limits. Test sensitivities (all tests) ranged from 42.8% to 62.4%; specificities ranged from 77.4% to 85.8%. For SAECG, sensitivity was 62% and specificity was 77%. A 3-stage stratification yielded a low-risk group (80.0% with a 2-year MAE risk of 2.9%), a high-risk group (11.8% with a 41.4% risk), and an unstratified group (8.2% with an 8.9% risk equivalent to a 2-year incidence of 7.9%). The authors concluded that sensitivities and specificities for the 5 tests were relatively similar and no test alone was satisfactory for predicting risk. Combinations of tests in stages allowed the authors to stratify 92% of patients as either high risk or low risk. The authors noted that these data suggest that a large prospective study to develop a robust prediction model is feasible and desirable.
The 2006 ACC, American Heart Association, and European Society of Cardiology guidelines for management of patients with ventricular arrhythmias and prevention of sudden death list SAECG with a Class IIb recommendation (Class IIb noted as usefulness/efficacy is less well established by evidence/opinion) (Zipes, 2006). The report notes that SAECG may be useful to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or of those at risk for life-threatening ventricular arrhythmias.
A recent consensus document from the American Heart Association, ACC Foundation, and Heart Rhythm Society indicates the SAECG may identify patients with prior MI at risk for sudden cardiac death and that further studies are required to assess the utility of this test (Goldberger, 2008).  
2012 Update
A search of the MEDLINE database was conducted through August 2012 did not reveal any new literature that would prompt a change in the coverage statement. A systematic review was identified assessing signal average ECG for the evaluation of acute coronary syndrome in patients with low to intermediate risk for coronary artery disease (Coeytaux, 2012). The authors conclude that further research is needed to better understand the clinical application and value of signal average ECG in patients with symptoms of acute coronary syndrome. “The comparative technical efficacy and diagnostic accuracy efficacy of these technologies as well as their impact on clinical decisionmaking and patient outcomes….is uncertain” (Coeytaux, 2012). The policy statement is unchanged.
2013 Update
A literature search using the MEDLINE database through August 2013 did not reveal any new information that would prompt a change in the coverage statement. The following is  a summary of the key identified literature.
In 2011, studies were also published on the utility of signal-averaged ECG for arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis, and epilepsy (Kamath, 2011; Rejdak, 2011; Schuller, 2011).  Kamath et al. tested the utility of signal-averaged ECG in diagnosing arrhythmogenic right ventricular cardiomyopathy (Kamath, 2011). These authors reported a sensitivity ranging from 47-69%, using different criteria for a positive test, and a specificity of 95%. Schuller et al. reported a sensitivity of 52% and specificity of 82% for detecting cardiac involvement in patients with sarcoidosis (Schuller, 2011). Rejdak et al. studied 45 consecutive patients with epilepsy and compared results of signal-averaged ECG with 19 healthy controls (Rejdak, 2011). An abnormal signal-averaged ECG was found in 48% (22/45) of patients with epilepsy compared with 5% (1/19) of control patients.
A number of studies have evaluated the use of p-wave signal averaged ECG to predict atrial arrhythmias. Militaru et al. performed p-wave signal-averaged ECG in 88 patients with paroxysmal atrial fibrillation, and compared the results to 330 normal subjects (Militaru, 2011). The patients with atrial fibrillation had a significantly longer p-wave duration and a higher p-wave integral compared to normal subjects. Furukawa et al. evaluated p-wave signal averaged ECG in 20 patients with Brugada syndrome and 20 age- and gender-matched controls (Furukawa, 2011). These authors reported that patients with Brugada syndrome had a longer p-wave duration and a higher p-wave voltage compared to controls. The authors also noted substantial heterogeneity of these measures among the patients with Brugada syndrome. A study published in 2012 assessed the association of abnormal p-wave duration and complications during the acute course of myocardial infarction in 89 patients (Shturman, 2012). Abnormal p-wave duration correlated with complications such as ventricular arrhythmias, heart failure, atrial fibrillation, and recurrent angina. However, it is uncertain whether knowledge of p-wave duration would meaningfully affect management of the patient and improve outcomes.
2014 Update
A literature search conducted through August 2014 did not reveal any new information that would prompt a change in the coverage statement. No trials were found where prospective use of SAECG was shown to improve outcomes. Thus, the policy statement remains unchanged.
2015 Update
A literature search conducted using the MEDLINE database through August 2015 did not reveal any new information that would prompt a change in the coverage statement.
2016 Update
A literature search conducted through August 2016 did not reveal any new information that would prompt a change in the coverage statement. The key identified literature is summarized below.
Liao and colleagues published a study on signal averaged electrocardiogram (SAECG) is a specific and non-invasive tool useful for arrhythmogenic right ventricular cardiomyopathy (ARVC) diagnosis. However, its role in risk stratification of patients with ARVC remains largely undefined (Liao, 2014). Sixty-four patients fulfilling Task Force ARVC criteria (mean age: 47 ± 14 years-old, 56% male, 50% definite ARVC) were enrolled. The baseline demographic, electrocardiographic, structural, and electrophysiological characteristics were collected. Patients with SAECG fulfilling all 3 Task Force criteria (3+ SAECG) were categorized into group 1, and those fulfilled 2 or less criterion were categorized into group 2. The study endpoints were unstable ventricular arrhythmia (VA), device detectable sustained fast VA (cycle lengths < 240 ms) and cardiovascular death. During a mean follow-up of 21 ± 20 months, 15 primary endpoints including 12 unstable VAs and 3 device-detected fast VAs were met. One patient died of electrical storm, and one patient underwent heart transplantation. The presence of 3+ SAECG predicted malignant events in all patients with definite and non-definite ARVC (p < 0.01, OR = 30.5, 95% CI = 2.5-373.7) and in patients with definite ARVC alone (p = 0.03, OR = 11.1, 95% CI = 1.3-93.9). Patients diagnosed with non-definite ARVC without 3+ SAECG were free from malignant events.
Zaidi and colleagues published a study with a goal to assess the accuracy of diagnostic criteria for ARVC when applied to athletes exhibiting electrocardiographic TWI and to identify discriminators between physiology and disease (Zaidi, 205). The study population consisted of athletes with TWI (n = 45), athletes without TWI (n = 35), and ARVC patients (n = 35). Subjects underwent electrocardiography (ECG), signal-averaged electrocardiography (SAECG), echocardiography, cardiac magnetic resonance imaging (CMRI), Holter monitoring, and exercise testing. There were no electrical, structural, or functional cardiac differences between athletes exhibiting TWI and athletes without TWI. When athletes were compared with ARVC patients, markers of physiological remodeling included early repolarization, biphasic TWI, voltage criteria for right ventricular (RV) or left ventricular hypertrophy, and symmetrical cardiac enlargement. Indicators of RV pathology included the following: syncope; Q waves or precordial QRS amplitudes <1.8 mV; 3 abnormal SAECG parameters; delayed gadolinium enhancement, RV ejection fraction ≤45%, or wall motion abnormalities at CMRI; >1,000 ventricular extrasystoles (or >500 non-RV outflow tract) per 24 h; and symptoms, ventricular tachyarrhythmias, or attenuated blood pressure response during exercise. Nonspecific parameters included the following: prolonged QRS terminal activation; ≤2 abnormal SAECG parameters; RV dilation without wall motion abnormalities; RV outflow tract ectopy; and exercise-induced T-wave pseudonormalization.
2017 Update
A literature search conducted through August 2017 did not reveal any new published results of  randomized controlled trials that would prompt a change in the coverage statement.
2018 Update
A literature search was conducted through August 2018.  There was no new information identified that would prompt a change in the coverage statement.  

93278Signal-averaged electrocardiography (SAECG), with or without ECG

References: Bailey JJ, Berson AS, Handelsman H et al.(2001) Utility of current risk stratification tests for predicting major arrhythmic events after myocardial infarction. J Am Coll Cardiol 2001; 38(7):1902-11.

Bauer A, Guzik P, et al.(2005) Reduced prognostic power of ventricular late potentials in post-infarction patients of the reperfusion era. Eur Heart J 2005; 26:755-61.

Bigger JT.(1997) Prophylactic use of implanted cardiac defibrillators in patients at high risk for ventricular arrhythmias after coronary artery bypass graft surgery. NEJM 1997; 337:1569-75.

Cain ME, et al.(1996) ACC expert consensus document. Signal averaged electrocardiography. JACC 1996; 27:238-49.

Cairns JA, et al.(1997) Randomized trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarization. Lancet 1997; 349:675-82.

Coeytaux R.R., Leisy P.J., Wagner G.S., et al.(2012) Systematic Review of ECG-based Signal Analysis Technologies for Evaluating Patients with Acute Coronary Syndrome. Technology Assessment Report by the Duke Evidence-based Practice Center for the Agency for Healthcare Research and Quality. Project ID: CRDD0311.

Furukawa Y, Yamada T, Okuyama Y et al.(2011) Increased intraatrial conduction abnormality assessed by P-wave signal-averaged electrocardiogram in patients with Brugada syndrome. Pacing Clin Electrophysiol 2011; 34(9):1138-46.

Goldberger JJ, Cain FM, Hohnloser SH et al.(2008) American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death. J Am Coll Cardiol 2008; 52:1179-99.

Goldberger JJ, Cain ME, et al.(2008) AHA/ACCF/HRS scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death: a scientific statement from the AHA, CCCEA & CEP. J Am Coll Cardiol, 2008; 52:1179-1199.

Gregoratos G, et al.(1998) ACC/AHA guidelines for implantation of cardiac pacemakers and antiarrhythmia devices; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Committee on Pacemaker Implantation. JACC 1998; 31;1175-1209.

Grimm W, Christ M, et al.(2003) Noninvasive arrhythmia risk stratification in idiopathic dilated cardiomyopathy. Circulation 2003; 108:2883-91.

Hohnloser SH, et al.(1999) Identification of patients after myocardial infarction at risk of life-threatening arrhythmias. Eur Heart J 1999; 1Suppl C:C11-20.

Huikuri HV, Tapanainen JM, et al.(2003) Prediction of sudden cardiac death after myocardial infarction in the beta-blocking era. J Am Coll Cardiol 2003; 42:652-8.

Julian DG, Camm AJ, Frangin G, et al.(1997) Randomized trial effect of amiodarone on mortality in patient with left ventricular dysfunction after recent myocardial infarction. Lancet 1997; 349:667-74.

Kamath GS, Zareba W, Delaney J et al.(2011) Value of the signal-averaged electrocardiogram in arrhythmogenic right ventricular cardiomyopathy/dysplasia. Heart Rhythm 2011; 8(2):256-62.

Klein H, et al.(1999) New primary prevention trials of sudden cardiac death in patients with left ventricular dysfunction. Am J Cardiol 1999; 83:91D-97D.

Koser LM, et al.(2000) Clinical significance of variability of ventricular late potentials detected before discharge in patients after myocardial infarction. Am Hrt J 2000; 139:134-41.

Liao YC, Lin YJ, Chung FP, et al.(2014) Risk stratification of arrhythmogenic right ventricular cardiomyopathy based on signal averaged electrocardiograms. Int J Cardiol. 2014 Jul 1;174(3):628-33.

Militaru C, Donoiu I, Ionescu DD.(2011) P Wave Signal-Averaged ECG in Normal Population and in Patients with Converted Atrial Fibrillation. Ann Noninvasive Electrocardiol 2011; 16(4):351-6.

Moss AJ, et al.(1996) Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. NEJM 1996; 335:1933-40.

Rejdak K, Rubaj A, Glowniak A et al.(2011) Analysis of ventricular late potentials in signal-averaged ECG of people with epilepsy. Epilepsia 2011; 52(11):2118-24.

Schuller JL, Lowery CM, Zipse M et al.(2011) Diagnostic utility of signal-averaged electrocardiography for detection of cardiac sarcoidosis. Ann Noninvasive Electrocardiol 2011; 16(1):70-6.

Shturman A, Bickel A, Atar S.(2012) The predictive value of P-wave duration by signal-averaged electrocardiogram in acute ST elevation myocardial infarction. The Israel Medical Association journal : IMAJ 2012; 14(8):493-7.

Strickberger SA, Benson DW, et al.(2006) AHA/ACCF Scientific Statement on the Evaluation of Syncope. J Am Coll Cardiol, 2006; 47:473-84.

Toubol P.(1999) A decade of clinical trials; CAST to AVID. Eur Heart J 1999; 1(sup C): C2-C10.

Ueno A, Kobayashi Y, Yodogawa K et al.(2007) A prospective study on the risk-stratification for patients with non-sustained ventricular tachycardia using a novel algorithm. Circ J 2007; 71(7):107-14.

US Department of HHS; Health Technology Assessment.(1998) Signal-averaged electrocardiography. Publication #PB98-137227 1998.

Zaidi A, Sheikh N, Jongman JK, et al.(2015) Clinical Differentiation Between Physiological Remodeling and Arrhythmogenic Right Ventricular Cardiomyopathy in Athletes With Marked Electrocardiographic Repolarization Anomalies. J Am Coll Cardiol. 2015 Jun 30;65(25):2702-11

Zipes DP, Camm AJ, Borggrefe M et al.(2006) ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Circulation 2006; 114(10):1088-132.

Zipes DP, Camm AJ, et al.(2006) ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. J Am Coll Cardiol, 2006; 48:247-346.

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